Only in the instance of the hyperfunctioning adrenal cortical adenoma with Cushing's syndrome is the uptake of the /sup 131/I-19iodocholesterol markedly decreased to absent in the adrenal cortices outside the adenoma. The mechanism for this lack of function outside the hyperfunctioning adrenal cortical adenoma presumably is suppression of pituitary ACTH by cortisol excess from the adrenal cortical adenoma resulting in subnormal stimulation of normal adrenocortical tissue. We report the occurrence of hyperactivity in one adrenal gland presumably from a functioning nodule, resulting in increased uptake with suppressed uptake of /sup 131/I-l9-iodocholesterol in the contralateral adrenal cortex in the absence of Cushing's syndrome. One 67-year-old woman had diabetes mellitus, a massively fatty liver, a dexamethasone nonsuppressible uptake of /sup 131/I-19-iodocholesterol in her right adrenal nodule, and a normal response to ACTH stimulation of the opposite adrenal gland. A 21-year-old woman had obesity, diabetes, progressive hirsuitism, sterility, and slightly elevated urinary 17- ketosteroid excretion. The increased uptake in the hot nodule in the right adrenal was suppressible with dexamethasone and ACTH produced a normal uptake in the opposite adrenal gland. The similarity of these functional nodules in more » the adrenal cortices to functional nodules previously observed in the thyroid gland with /sup 131/I is apparent. (auth) « less